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    Wyświetlanie 1-6 z 6
    Tytuł:
    The involvement of RIPK4 in TNF-$\alpha$-stimulated IL-6 and IL-8 production by melanoma cells
    Autorzy:
    Brożyna, Anna A.
    Wolnicka-Głubisz, Agnieszka
    Lisek, Anna
    Deptula, Milena
    Madej, Ewelina
    Wroński, Norbert
    Wardowska, Anna
    Cierniak, Agnieszka
    Opis:
    Purpose The receptor-interacting protein kinase (RIPK4) has an oncogenic function in melanoma, regulates NF-$\kappa$B and Wnt/$\beta$-catenin pathways, and is sensitive to the BRAF inhibitors: vemurafenib and dabrafenib which lead to its decreased level. As its role in melanoma remains not fully understood, we examined the effects of its downregulation on the transcriptomic profile of melanoma. Methods Applying RNA-seq, we revealed global alterations in the transcriptome of WM266.4 cells with RIPK4 silencing. Functional partners of RIPK4 were evaluated using STRING and GeneMANIA databases. Cells with transient knockdown (via siRNA) and stable knockout (via CRISPR/Cas9) of RIPK4 were stimulated with TNF-$\alpha$. The expression levels of selected proteins were assessed using Western blot, ELISA, and qPCR. Results Global analysis of gene expression changes indicates a complex role for RIPK4 in regulating adhesion, migration, proliferation, and inflammatory processes in melanoma cells. Our study highlights potential functional partners of RIPK4 such as BIRC3, TNF-$\alpha$ receptors, and MAP2K6. Data from RIPK4 knockout cells suggest a putative role for RIPK4 in modulating TNF-$\alpha$-induced production of IL-8 and IL-6 through two distinct signaling pathways—BIRC3/NF-$\kappa$B and p38/MAPK. Furthermore, increased serum TNF-$\alpha$ levels and the correlation of RIPK4 with NF-$\kappa$B were revealed in melanoma patients. Conclusion These data reveal a complex role for RIPK4 in regulating the immune signaling network in melanoma cells and suggest that this kinase may represent an alternative target for melanoma-targeted adjuvant therapy.
    Dostawca treści:
    Repozytorium Uniwersytetu Jagiellońskiego
    Artykuł
    Tytuł:
    Atrioventricular node dysfunction in pressure overload-induced heart failure - involvement of the immune system and transcriptomic remodelling
    Autorzy:
    D'Souza, Alicia
    Dobrzynski, Halina
    Zi, Min
    Hussain, Munir
    Wilson, Claire
    Boyett, Mark R.
    Smith, Matthew
    Opis:
    Heart failure is associated with atrioventricular (AV) node dysfunction, and AV node dysfunction in the setting of heart failure is associated with an increased risk of mortality and heart failure hospitalisation. This study aims to understand the causes of AV node dysfunction in heart failure by studying changes in the whole nodal transcriptome. The mouse transverse aortic constriction model of pressure overload-induced heart failure was studied; functional changes were assessed using electrocardiography and echocardiography and the transcriptome of the AV node was quantified using RNAseq. Heart failure was associated with a significant increase in the PR interval, indicating a slowing of AV node conduction and AV node dysfunction, and significant changes in 3,077 transcripts (5.6% of the transcriptome). Many systems were affected: transcripts supporting AV node conduction were downregulated and there were changes in transcripts identified by GWAS as determinants of the PR interval. In addition, there was evidence of remodelling of the sarcomere, a shift from fatty acid to glucose metabolism, remodelling of the extracellular matrix, and remodelling of the transcription and translation machinery. There was evidence of the causes of this widespread remodelling of the AV node: evidence of dysregulation of multiple intracellular signalling pathways, dysregulation of 109 protein kinases and 148 transcription factors, and an immune response with a proliferation of neutrophils, monocytes, macrophages and B lymphocytes and a dysregulation of 40 cytokines. In conclusion, inflammation and a widespread transcriptional remodelling of the AV node underlies AV node dysfunction in heart failure.
    Dostawca treści:
    Repozytorium Uniwersytetu Jagiellońskiego
    Artykuł
      Wyświetlanie 1-6 z 6

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